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Understanding resistance to EGFR inhibitors—impact on future treatment strategies
Open accessAbstract
EGFR is a tyrosine kinase that participates in the regulation of cellular homeostasis. Following ligand binding, EGFR stimulates downstream cell signaling cascades that influence cell proliferation, apoptosis, migration, survival and complex processes, including angiogenesis and tumorigenesis. EGFR has been strongly implicated in the biology of human epithelial malignancies, with therapeutic applications in cancers of the colon, head and neck, lung, and pancreas. Accordingly, targeting EGFR has been intensely pursued, with the development of a series of promising molecular inhibitors for use in clinical oncology. As is common in cancer therapy, challenges with respect to treatment resistance emerge over time. This situation is certainly true of EGFR inhibitor therapies, where intrinsic and acquired resistance is now well recognized. In this Review, we provide a brief overview regarding the biology of EGFR, preclinical and clinical development of EGFR inhibitors, and molecular mechanisms that underlie the development of treatment resistance. A greater understanding of the mechanisms that lead to EGFR resistance may provide valuable insights to help design new strategies that will enhance the impact of this promising class of inhibitors for the treatment of cancer.
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“Therefore, other PI3K pathway activating lesions commonly found in GBM, such as the activation of other RTKs (6, 12, 39), could also promote increased LDLR expression.”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [39]
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Metadata
- Authors
- Wheeler, D. L., Dunn, E. F., & Harari, P. M.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Wheeler, Deric L.
- Venue
- Nature Reviews Clinical Oncology
- Published
- 2010-06-15
- Volume
- 7
- Issue
- 9
- Pages
- 493-507
- ISSN
- 1759-4774 (ISSN-L)
- 1759-4782
- PMC
- PMC2929287
- OpenAlex
- W2053439872
- Cited by
- 683
- References
- 182
- Citations by year
- 2026: 21 · 2025: 20 · 2024: 35 · 2023: 29 · 2022: 31 · 2021: 29 · 2020: 44 · 2019: 25 · 2018: 36 · 2017: 50 · 2016: 46 · 2015: 61 · 2014: 66 · 2013: 68 · 2012: 64
- FWCI
- 6.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Clinical Oncology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5t32ca009614-25)
- U.S. Public Health Service (P30CAO14520)
- National Cancer Institute (T-32 CA 0096-14, R01CA113448)
- National Center for Research Resources (UL1RR025011)
- Topics
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Keywords
- EGFR inhibitors, EGFR, acquired drug resistance, intrinsic resistance, tyrosine kinase inhibitors, resistance mechanisms, EGFR signaling, epithelial malignancies, lung cancer, head and neck cancer, colon cancer, pancreatic cancer, combination therapy
- MeSH terms
- Cetuximab, Erlotinib Hydrochloride, Gefitinib, Panitumumab, Antibodies, Monoclonal, Antineoplastic Agents, Humans, Neoplasms, Proto-Oncogene Proteins, Quinazolines, Proto-Oncogene Proteins p21(ras), Treatment Outcome, Disease Progression, ras Proteins, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, Antibodies, Monoclonal, Humanized, ErbB Receptors
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